Neurophysiological correlates of the dopaminergic cilio-inhibitory mechanism of Mytilus edulis

The neurophysiological regulation of gill ciliary activity by the CNS of the bivalve mollusc Mytilus edulis was studied by recording electrophysiological activity of the branchial nerve while simultaneously observing ciliary activity of the lateral ciliated cells of the gill by stroboscopic microscopy. The addition of dopamine to the visceral ganglion slowed and stopped ciliary activity by increasing the firing rate of the cilio-inhibitory dopaminergic neurones of the visceral ganglion which innervate the gill. This could be antagonized at the ganglion by pre-applications of ergonovine or methysergide, or by prior treatments of intact animals with the neurotoxin 6-hydroxydopamine. The study confirms earlier work showing the inhibitory functioning of dopaminergic neurones of the CNS and demonstrates the manner in which they may exert their effects.

The coordinate roles of branchial nerve activity and potassium in the stimulation of ciliary activity in Mytilus edulis: observations with phenoxybenzamine, bromolysergic acid and fluorescence histochemistry

Potassium concentrations in excess of 30 mM increase the rate of beating of lateral cilia on the gill of Mytilus edulis. Cilioexcitation produced by low frequency (5 beats/s) electrical stimulation was potentiated with potassium but blocked with bromolysergic acid (a serotonergic inhibitor). Cilioinhibition produced by high frequency (50 beats/s) stimulation was decreased with potassium and phenoxybenzamine (a dopaminergic inhibitor). Phenoxybenzamine enhanced the cilioexcitation produced by potassium. Potassium doses incapable of maintaining a basal rate of beating (less than 30 mM) could increase ciliary activity if phenoxybenzamine was also added. After transection of the branchial nerve, the yellow-fluorophore (serotonergic storage) and cilioexcitatory effect of potassium gradually decrease. This study shows that the potassium effect on ciliary activity (a) increase with low frequency nerve stimulation, presumably through the release of serotonin and (b) decreases with high frequency nerve stimulation, presumably through the release of dopamine.